Secretion Of Gastrointestinal Peptides Research Articles

Effects of Dietary Chromium Picolinate on Gut Microbiota, Gastrointestinal Peptides, Glucose Homeostasis, and Performance of Heat-Stressed Broilers.

Simple SummaryHigh ambient temperature is a common environmental issue in poultry breeding. It not only seriously damaged the growth performance of broilers, but also had adverse effects on intestinal microbial composition, gastrointestinal peptide, and glucose homeostasis. Trivalent chromium has the ability to improve the absorption and utilization of glucose. To date, the impacts of trivalent chromium on the above indexes remain only partially clear. This research discussed the influence of chromium supplementation on performance, microbiota, gastrointestinal peptides, and glucose homeostasis in heat-stressed broilers.The current research was devoted to evaluating the effects on gut microbiota, gastrointestinal peptides, and glucose homeostasis of chromium picolinate applied to heat-stressed broilers. In a 14 d experiment, 220 28-day-old AA broilers were randomly assigned into one thermal-neutral and three high-temperature groups dietary-supplemented with 0, 0.4, or 0.8 mg/kg of chromium as chromium picolinate. The temperature for the thermal-neutral group was set at 21 °C, while that for the other three groups (high temperature) was set at 31 °C. The results showed that the average daily gain and average daily feed intake of the 0.4 mg/kg chromium-supplemented group significantly increased compared with the high-temperature groups (p < 0.05). The content of cholecystokinin in the 0.4 mg/kg group significantly decreased, and the gastric inhibitory polypeptide level was significantly elevated in jejunum (p < 0.05). The cecal microbiota of heat-stressed broilers was substantially different from that of the thermal-neutral group. After diet-supplemented chromium, compared to the high-temperature groups, the 0.4 mg/kg chromium supplemented group was characterized by a reduction of Actinobacteriota and Proteobacteria at the phylum level. The Bacilli were elevated, while proportions of Coriobacteria and Gammaproteobacteria were reduced significantly at the class level. The proportions of Lactobacillaceae, Christensenellaceae, and Erysipelotrichaceae were elevated significantly, while that of Clostridiaceae was reduced significantly at the family level. The proportion of Turicibacter was elevated significantly and the proportions of Olsenella and Ruminococcus were reduced significantly at the genus level (p < 0.05). Compared to the high-temperature groups, in the 0.4 mg/kg chromium-supplemented group, the insulin concentration and insulin resistance index were reduced (p < 0.05), and sodium-glucose transporter 1 expression was up-regulated in jejunum (p < 0.05). Performance, microbiota, gastrointestinal peptides, or serum parameters of the 0.8 mg/kg group were almost unaffected by chromium compared with the high-temperature groups. In conclusion, diet supplemented with 0.4 mg/kg Cr improved performance, insulin resistance and sodium-glucose transporter 1 expression and altered gut microflora structure and secretion of gastrointestinal peptides, thus showing that supplementation with chromium is beneficial to maintain glucose homeostasis and alleviate heat stress.

Seasonal expressions of GPR41 and GPR43 in the colon of the wild ground squirrels (Spermophilus dauricus).

G-protein-coupled receptor 41 (GPR41) and G-protein-coupled receptor 43 (GPR43) are important short-chain fatty acids (SCFAs) receptors. Previous studies indicated that GPR41 and GPR43 are involved in the secretion of gastrointestinal peptides, and glucose and lipid metabolism, and are closely related to obesity and type II diabetes, and other diseases. The purpose of the study was to explore the relationship of the GPR41 and GPR43 with seasonal breeding, and provide new prospects for further exploring the nutritional needs of breeding. We identified the localization and expression levels of GPR41 and GPR43 in the colon of the wild ground squirrels (Spermophilus dauricus) both in the breeding season and non-breeding season. The histological results revealed that the lumen diameter of the colon had obvious seasonal changes, and the diameter of the colonic lumen in the non-breeding season was larger than that in the breeding season. Immunohistochemical staining suggested that GPR41 and GPR43 are expressed in the simple layer columnar epithelium. In addition, compared with the breeding season, the mRNA and protein expression levels of GPR41 and GPR43 in the colon were higher during the non-breeding season. In general, these results indicated that GPR41 and GPR43 might play a certain role in regulating seasonal breeding.

GPR43 regulation of mitochondrial damage to alleviate inflammatory reaction in sepsis.

Sepsis is a common critical illness in ICU and always a great difficulty in clinical treatment. GPR43 (G protein-coupled receptor 43) participates in regulating appetite and gastrointestinal peptide secretion to modulate fat decomposition and formation. However, the biological contribution of GPR43 on inflammation of sepsis has not been previously investigated. We investigated the mechanisms of GPR43 gene, which plays a possible role in distinguishing sepsis and contributes to the pathogenesis of sepsis-induced inflammatory reaction. Furthermore, we performed studies with mice induced to sepsis by Cecal Ligation and Puncture (CLP), Knockout GPR43 (GPR43-/-) mice, and Wild Type (WT) mice induced with CLP. In addition, lung tissues and cell samples were analyzed by histology, Quantitative Polymerase Chain Reaction (Q-PCR), Enzyme-linked Immunosorbent (ELISA) Assay, and western blot. GPR43 agonist could significantly reduce inflammation reactions and trigger lung injury in mice with sepsis. As for GPR43-/- mice, the risks of sepsis-induced inflammatory reactions and corresponding lung injury were promoted. On the one hand, the up-regulation of GPR43 gene reduced ROS mitochondrial damage to inhibit inflammatory reactions via the inactivation of NLRP3 Inflammasome by PPARγ/ Nox1/EBP50/ p47phox signal channel. On the other hand, the down-regulation of GPR43 promoted inflammatory reactions in vitro model through the acceleration of ROS-dependently mitochondrial damage by PPARγ/ Nox1/EBP50/ p47phox/ NLRP3 signal channel. These findings indicate that the inhibition of GPR43 as a possible important factor of sepsis may shed lights on the mechanism of sepsis-induced inflammation reaction.

Evaluation of an amino acid mix on the secretion of gastrointestinal peptides, glucometabolic homeostasis, and appetite in obese adolescents administered with a fixed-dose or ad libitum meal

Evaluation of an amino acid mix on the secretion of gastrointestinal peptides, glucometabolic homeostasis, and appetite in obese adolescents administered with a fixed-dose or ad libitum meal

Gut peptides and the microbiome: focus on ghrelin.

Purpose of reviewIn this review, we present recent insights into the role of the gut microbiota on gastrointestinal (GI) peptide secretion and signalling, with a focus on the orexigenic hormone, ghrelin.Recent findingsEvidence is accumulating suggesting that secretion of GI peptides is modulated by commensal bacteria present in our GI tract. Recent data shows that the gut microbiome impacts on ghrelinergic signalling through its metabolites, at the level of the ghrelin receptor (growth hormone secretagogue receptor) and highlights concomitant changes in circulating ghrelin levels with specific gut microbiota changes. However, the mechanisms by which the gut microbiota interacts with gut peptide secretion and signalling, including ghrelin, are still largely unknown.SummaryThe gut microbiota may directly or indirectly influence secretion of the orexigenic hormone, ghrelin, similar to the modulation of satiety inducing GI hormones. Although data demonstrating a role of the microbiota on ghrelinergic signalling is starting to emerge, future mechanistic studies are needed to understand the full impact of the microbiota-ghrelin axis on metabolism and central-regulated homeostatic and non-homeostatic controls of food intake.

Evaluation of an Amino Acid Mix on the Secretion of Gastrointestinal Peptides, Glucometabolic Homeostasis, and Appetite in Obese Adolescents Administered with a Fixed-Dose or ad Libitum Meal

Proteins have been demonstrated to reduce food intake in animals and humans via peripheral and central mechanisms. Supplementation of a dietetic regimen with single or mixed amino acids might represent an approach to improve the effectiveness of any body weight reduction program in obese subjects. The aim of the present study was to evaluate the effects of an amino acid mix (L-arginine + L-leucine + L-glutamine + L-tryptophan) on the secretion of some gastrointestinal peptides (i.e., ghrelin and glucagon-like peptide type 1, GLP-1), glucometabolic homeostasis (i.e., glucose, insulin, and glucagon), and appetite (hunger/satiety scored by visual analogue scale, VAS) in obese adolescents (n = 14; 10 females and 4 males; age: 16.6 ± 1.0 years; body mass index (BMI): 36.4 ± 4.6 kg/m²; fat-free mass (FFM): 54.9 ± 4.7%; fat mass (FM): 45.1 ± 4.4%) administered with a fixed-dose (lunch) or ad libitum (dinner) meal. Isocaloric maltodextrins were used as control treatment. During the lunch test, a significant increase in circulating levels of GLP-1, but not of ghrelin, was observed in the amino acid-treated group, which was congruent with significant changes in appetite, i.e., increase in satiety and decrease in hunger. A significant hyperglycemia was found in the maltodextrin-treated group during the prelunch period, without any significant changes in insulin and glucagon between the two groups. During the dinner test, there were no significant differences in appetite (hunger/satiety) and intake of calories. In conclusion, L-arginine, L-leucine, L-glutamine, and L-tryptophan, when administered to obese adolescents with a fixed-dose meal, are capable of evoking an anorexigenic response, which is, at least in part, mediated by an increase in GLP-1 released in circulation by L cells, which are capable of chemosensing specific amino acids present in the intestinal lumen. Further additional studies are requested to understand whether higher doses are necessary to inhibit ad libitum feeding.

Inorganic mesoporous particles for controlled α-linolenic acid delivery to stimulate GLP-1 secretion in vitro

Novel treatment methods for obesity are urgently needed due to the increasing global severity of the problem. Gastrointestinal hormones, such as GLP-1 and PYY, are secreted by the enteroendocrine cells, playing a critical role in regulating food intake. Digested nutrients trigger the secretion of these hormones, which have a very short half-life. α-Linolenic acid (αLA) has been shown to stimulate GLP-1 secretion, however, chemical instability and fast uptake in the small intestine hinder its use in body weight management. We developed a novel delivery system based on inorganic mesoporous particles for αLA to increase secretion of gastrointestinal peptides. αLA was loaded to thermally hydrocarbonized porous silicon particles (THCPSi). 47.9 ± 3.84% and 30.7 ± 2.86% of αLA was released during 6 h from 3.0% and 9.2% loading degree (w/w) samples in vitro, respectively. Native αLA (50 µM) significantly increased GLP-1 secretion from enteroendocrine STC-1 and GLUTag cell lines. αLA loaded THCPSi significantly and dose dependently stimulated GLP-1 secretion from STC-1 cells, whereas empty particles did not. We demonstrated in vitro that THCPSi particles have the potential to be used as a controlled delivery system for nutrients such as αLA, increasing GLP-1 secretion. Our results justify further in vivo investigations.

Contribution of Vladimir Kharitonovich Vasilenko and his disciples to the study of ulcer disease

The article outlines the contribution of V.Kh. Vasilenko and his disciples to the study of ulcer disease including substantiation of its pathogenesis as a result of disbalance between the aggressive action of acidic and peptic factors and protective potential of gastric and duodenal mucosa based on the evaluation of their role in mucus production, epithelial cell regeneration, secretion of gastrointestinal peptides, and other processes. Special emphasis is laid on the differentiation between ulcer disease and symptomatic gastroduodenal ulcers as proposed by Vasilenko, his analysis of the clinical picture and diagnostics of ulcer disease depending on the patient’s age and sex, evaluation of therapeutic efficiency of antiulcer medicines. Recent literature data confirm Vasiolenko’s idea about different role of selected pathogenic factors in individual patients with ulcer disease.

Control of Food Intake by Gastrointestinal Peptides: Mechanisms of Action and Possible Modulation in the Treatment of Obesity.

This review focuses on the control of appetite by food intake-regulatory peptides secreted from the gastrointestinal tract, namely cholecystokinin, glucagon-like peptide 1, peptide YY, ghrelin, and the recently discovered nesfatin-1 via the gut-brain axis. Additionally, we describe the impact of external factors such as intake of different nutrients or stress on the secretion of gastrointestinal peptides. Finally, we highlight possible conservative—physical activity and pharmacotherapy—treatment strategies for obesity as well as surgical techniques such as deep brain stimulation and bariatric surgery also altering these peptidergic pathways.

Neuroendocrinology of Adipose Tissue and Gut-Brain Axis.

Food intake and energy expenditure are closely regulated by several mechanisms which involve peripheral organs and nervous system, in order to maintain energy homeostasis.Short-term and long-term signals express the size and composition of ingested nutrients and the amount of body fat, respectively. Ingested nutrients trigger mechanical forces and gastrointestinal peptide secretion which provide signals to the brain through neuronal and endocrine pathways. Pancreatic hormones also play a role in energy balance exerting a short-acting control regulating the start, end, and composition of a meal. In addition, insulin and leptin derived from adipose tissue are involved in long-acting adiposity signals and regulate body weigh as well as the amount of energy stored as fat over time.This chapter focuses on the gastrointestinal-, pancreatic-, and adipose tissue-derived signals which are integrated in selective orexigenic and anorexigenic brain areas that, in turn, regulate food intake, energy expenditure, and peripheral metabolism.

Macronutrients, food intake and body weight; the role of fat

"Globesity" is the term that the World Health Organization (WHO) employs to define the growth of obesity in the world from the last 40 years which started in the developed countries and has been inevitably propagated to the developing ones. Governments and international organizations are aware of the problem and they are trying to implement measures to fight it. To analyze the current evidence in terms of studies about the relationship between macronutrients (especially fat and lipid release systems) and the secretion of gastrointestinal peptides that are involved with satiety and satiation. The search was conducted in Medline (via Pubmed) using different combinations of MeSH terms and in the database LILACs using "DeCS". A selection of another articles relevant to the review topic was also examined. At present, there are several laboratories and industries developing novel bioactive ingredients aimed at the regulation of food intake, with emphasis on those related with fat intake and the different ways in which fat can be technologically processed in order to create structures able to enhance satiety and/ or diminish hunger. These ingredients will be the future of functional foods focused on the prevention of weight gain and the support of other strategies against obesity (dietary, behavioral, etc…).

Omega-3 Fatty Acids and FFAR4.

The beneficial roles of omega-3 fatty acids (ω3-FAs) on obesity, type 2 diabetes, and other metabolic diseases are well known. Most of these effects can be explained by their anti-inflammatory effects triggered through their receptor, free fatty acid receptor 4 (FFAR4) activation. Although the whole mechanism of action is not fully described yet, it has been shown that stimulation of ω3-FA to FFAR4 is followed by receptor phosphorylation. This makes FFAR4 to be capable of interacting with β-arrestin-2, which in turn, results in association of β-arrestin-2 with TAB1. This stealing of an important partaker of the inflammatory cascade leads to interruption of the pathway, resulting in reduced inflammation. Besides this regulation of the anti-inflammatory response, FFAR4 signaling also has been shown to regulate glucose homeostasis, adiposity, gastrointestinal peptide secretion, and taste preference. In this review, we summarize the current knowledge about the interaction of ω3-FAs with FFAR4 and the consequent opportunities for the application of ω3-FAs and possible FFAR4 targets.

Ileal brake activation: macronutrient-specific effects on eating behavior?

Activation of the ileal brake, by infusing lipid directly into the distal part of the small intestine, alters gastrointestinal (GI) motility and inhibits food intake. The ileal brake effect on eating behavior of the other macronutrients is currently unknown. The objective of this study was to investigate the effects of ileal infusion of sucrose and casein on food intake, release of GI peptides, gastric emptying rate and small-bowel transit time with safflower oil as positive control. This randomized, single-blind, crossover study was performed in 13 healthy subjects (6 male; mean age 26.4±2.9 years; mean body mass index 22.8±0.4 kg m(-2)) who were intubated with a naso-ileal catheter. Thirty minutes after the intake of a standardized breakfast, participants received an ileal infusion, containing control ((C) saline), safflower oil ((HL) 51.7 kcal), low-dose casein ((LP) 17.2 kcal) or high-dose casein ((HP) 51.7 kcal), low-dose sucrose ((LC) 17.2 kcal) and high-dose sucrose ((HC) 51.7 kcal), over a period of 90 min. Food intake was determined during an ad libitum meal. Visual analogue score questionnaires for hunger and satiety and blood samples were collected at regular intervals. Ileal infusion of lipid, protein and carbohydrate resulted in a significant reduction in food intake compared with control (HL: 464.3±90.7 kcal, P<0.001; HP: 458.0±78.6 kcal, P<0.005; HC: 399.0±57.0 kcal, P<0.0001 vs control: 586.7±70.2 kcal, P<0.001, respectively). A reduction in energy intake was still apparent when the caloric amount of infused nutrients was added to the amount eaten during the ad libitum meal.Secretion of cholecystokinin and peptide YY but not of glucagon-like peptide-1 (7-36) was increased during ileal perfusion of fat, carbohydrates and protein. During ileal perfusion of all macronutrients, a delay in gastric emptying and intestinal transit was observed, but differences were not significant compared with control. Apart from lipids, also sucrose and casein reduce food intake on ileal infusion, thereby activating the ileal brake. In addition to food intake, also satiety and GI peptide secretion were affected.

Gut sweet taste receptors and their role in metabolism.

Obesity is caused by an imbalance between food intake and energy expenditure. In recent decades the gastrointestinal tract has received growing attention as a control parameter for the regulation of appetite and food intake, however regulatory circuits and their interactions are complex. The basic understanding on the role of the gut starts with the notion 'we are what we eat'. Food enters the gastrointestinal tract, which then triggers specific mechanisms or a sensing machinery that respond to specific components of food. Enteroendocrine cells in the small intestine are the anatomical basis for the sensing machinery, which act as neural triggers or as intestinal satiation peptide-secreting cells. These cells express chemosensory receptors that respond to luminal stimuli. The understanding of each gastrointestinal mechanism that might be involved in the process of eating provides a basis for the assessment of the potential of the gastrointestinal tract in the fight against obesity. This review discusses the function of the gut sweet taste receptor T1R2/T1R3 in sensing sweet compounds, as well as its role in gastrointestinal peptide secretion and glucose metabolism.

GPR43 regulates metabolic function in skeletal muscle cells

Introduction: Preliminary data suggests a putative role for GPR43 in regulating systemic health via processes including adipogenesis, inflammation and secretion of gastrointestinal peptides. This suggests GPR43 may have a role in weight control. Given muscle is a major determinant of systemic metabolic health and energy balance, we sought to characterise the effect of activating GPR43 in skeletal and cardiac muscle cells. Methods: C2C12 skeletal muscle myotubes and H9c2 cardiac muscle myoblasts were exposed to a GPR43 specific phenylacetamide (PA) agonist (70 nM to 7 M) for 15min (n = 5—8/group). Protein expression was quantified by Western blotting. Metabolic activity of C2C12 and H9c2 cells treated with PA was determined via MTT assay (n = 10—12/group). Results: In C2C12 myotubes 70 nM PA significantly up-regulated total JNK and AMPK proteins compared to control (p≤ 0.05). There was no change in the phosphorylation of these markers or the abundance of total or phosphorylated ERK1/2 protein at any dose used. Metabolic activity in C2C12 myotubes was decreased at 70 nM and 7 M PA compared to control (p≤ 0.05). Interestingly, PA treatment did not alter protein expression or metabolic activity in H9c2 myoblasts. Conclusion: These data suggest GPR43 may have a specific role in mediating skeletal muscle metabolic function. Decrements in metabolic activity in C2C12 myotubes imply GPR43 agonism may impinge upon nutrient metabolism in skeletal muscle. This has the potential to promote aberrations of systemic metabolic health. Thus, targeting GPR43 may form a novel means of treating obesity and type 2 diabetes mellitus in which skeletal muscle fatty acid and glucose metabolism is perturbed. Further work is needed to clarify the signaling pathways mediating decreased metabolic activity and how this relates to functional changes in nutrient metabolism. LMC was supported by a scholarship (PB 10M 5472) from the National Heart Foundation of Australia.

The therapeutic potential of GPR43: a novel role in modulating metabolic health.

GPR43 is a receptor for short-chain fatty acids. Preliminary data suggest a putative role for GPR43 in regulating systemic health via processes including inflammation, carcinogenesis, gastrointestinal function, and adipogenesis. GPR43 is involved in secretion of gastrointestinal peptides, which regulate appetite and gastrointestinal motility. This suggests GPR43 may have a role in weight control. Moreover, GPR43 regulates plasma lipid profile and inflammatory processes, which further indicates that GPR43 could have the ability to modulate the etiology and pathogenesis of metabolic diseases such as obesity, type 2 diabetes mellitus, and cardiovascular disease. This review summarizes the current evidence regarding the ability of GPR43 to mediate both systemic and tissue specific functions and how GPR43 may be modulated in the treatment of metabolic disease.

Effects of carbohydrate sugars and artificial sweeteners on appetite and the secretion of gastrointestinal satiety peptides

In vitro, both carbohydrate sugars and artificial sweeteners (AS) stimulate the secretion of glucagon-like peptide-1 (GLP-1). It has been suggested that the gut tastes sugars and AS through the same mechanisms as the tongue, with potential effects on gut hormone release. We investigated whether the human gut responds in the same way to AS and carbohydrate sugars, which are perceived by lingual taste as equisweet. We focused on the secretion of gastrointestinal (GI) satiety peptides in relation to appetite perception. We performed a placebo-controlled, double-blind, six-way, cross-over trial including twelve healthy subjects. On separate days, each subject received an intragastric infusion of glucose, fructose or an AS (aspartame, acesulfame K and sucralose) dissolved in 250ml of water or water only (control). In a second part, four subjects received an intragastric infusion of the non-sweet, non-metabolisable sugar analogue 2-deoxy-d-glucose. Glucose stimulated GLP-1 (P=0·002) and peptide tyrosine tyrosine (PYY; P=0·046) secretion and reduced fasting plasma ghrelin (P=0·046), whereas fructose was less effective. Both carbohydrate sugars increased satiety and fullness (albeit not significantly) compared with water. In contrast, equisweet loads of AS did not affect gastrointestinal peptide secretion with minimal effects on appetite. 2-Deoxy-d-glucose increased hunger ratings, however, with no effects on GLP-1, PYY or ghrelin. Our data demonstrate that the secretion of GLP-1, PYY and ghrelin depends on more than the detection of (1) sweetness or (2) the structural analogy to glucose.

Role of Cardiac Steatosis and Lipotoxicity in Obesity Cardiomyopathy

See related article, pp 216–222 The pandemic of obesity is a devastating health problem and contributes to premature morbidity and mortality. Results from clinical and experimental studies have identified a variety of unfavorable consequences of obesity including cardiovascular diseases, pulmonary diseases, cancer, and sleep disorders. An obesity-triggered parallel increase in the prevalence of type 2 diabetes mellitus is also expected to add to the overall cardiovascular burden of obesity. Components of metabolic syndrome such as dyslipidemia, hyperglycemia, insulin resistance, and hypertension are thought to play pivotal roles in obesity-associated sequelae responsible for atherosclerosis, cardiac hypertrophy, and ventricular dysfunction. The presence of 1 or more of these metabolic syndrome components can adversely affect multiple metabolic pathways resulting in alterations in glucose and lipid metabolism, fatty acid (FA) transport/storage/oxidation, oxygen consumption, redox status, and high-energy phosphate metabolism. Although the precise mechanism(s) of action responsible for metabolic derangement-induced cardiac abnormalities in obesity remains poorly understood, 1 theory that has received increasing attention focuses on lipid transport and storage, excessive FA oxidation (FAO), and lipotoxic injury to the heart.1,2 When energy intake exceeds expenditure, fat is stored as triacylglycerol (TG) in adipose tissue. In turn, once fat levels exceed the storage capacity of adipocytes, a variety of neutral lipids are released and accumulated in other cells and tissues including the heart. The presence of lipid inclusions within cardiomyocytes, a condition referred to as cardiac steatosis, has been confirmed in obesity and diabetes.3,4 Although recent evidence indicates that cardiac steatosis, increased availability of FA and excess FAO contribute to cardiac anomalies associated with obesity and type 2 diabetes, it has also been suggested that cardiac steatosis may be a compensatory mechanism used to neutralize FAs and their metabolites through esterification to neutral lipids. Generation of ATP for normal cardiac …

Inulin-Type Fructans: Functional Food Ingredients

A food (ingredient) is regarded as functional if it is satisfactorily demonstrated to affect beneficially 1 or more target functions in the body beyond adequate nutritional effects. The term inulin-type fructans covers all β(2←1) linear fructans including native inulin (DP 2–60, DPav = 12), oligofructose (DP 2–8, DPav = 4), and inulin HP (DP 10–60, DPav = 25) as well as Synergy 1, a specific combination of oligofructose and inulin HP. Inulin-type fructans resist digestion and function as dietary fiber improving bowel habits. But, unlike most dietary fibers, their colonic fermentation is selective, thus causing significant changes in the composition of the gut microflora with increased and reduced numbers of potentially health-promoting bacteria and potentially harmful species, respectively. Both oligofructose and inulin act in this way and thus are prebiotic: they also induce changes in the colonic epithelium and in miscellaneous colonic functions. In particular, the claim “inulin-type fructans enhance calcium and magnesium absorption” is scientifically substantiated, and the most active product is oligofructose-enriched inulin (Synergy 1). A series of studies furthermore demonstrate that inulin-type fructans modulate the secretion of gastrointestinal peptides involved in appetite regulation as well as lipid metabolism. Moreover, a large number of animal studies and preliminary human data show that inulin-type fructans reduce the risk of colon carcinogenesis and improve the management of inflammatory bowel diseases. Inulin-type fructans are thus functional food ingredients that are eligible for enhanced function claims, but, as more human data become available, risk reduction claims will become scientifically substantiated.

The effect of antenatal corticosteroids on gut peptides of preterm infants—a matched group comparison: Corticosteroids and gut development

Background: Postnatal glucocorticosteroid administration has trophic effects on the gastrointestinal tract of preterm infants. The aim of the present study was to investigate whether antenatal glucocorticosteroids affect the secretion of gastrointestinal peptides that are involved in the regulation of secretion, motility and mucosal protection of the gastrointestinal tract. Methods: Plasma levels of gastrin, motilin and vasoactive intestinal peptide (VIP) were estimated in 28 preterm infants with a mean birth weight of 1280 g, and mean gestational age of 30.5 weeks, whose mothers had received a full course of antenatal glucocorticosteroids (GC group) and in 17 preterm infants with mean birth weight of 1200 g, mean gestational age of 30.2 weeks, whose mothers had not received corticosteroids (control group). GI peptides were estimated on two occasions: (a) Immediately after birth and (b) following the initiation of enteral feeding. Results: Gastrin levels in the GC group were significantly higher both immediately after birth (early measurement) and also after receiving enteral feeding (late measurement) ( p<0.001, p<0.05, respectively) but the increase in plasma gastrin concentration was identical in both groups (32 vs. 33 pg/ml). Motilin levels in the GC group were also significantly higher as compared to the control group but only in the late measurement ( p<0.001). Gastrin and motilin levels in both groups were significantly higher in the late measurement as compared to the early measurement (GC group: p<0.001, p<0.001, respectively; Controls: p<0.001, p<0.01, respectively). There was no significant difference in VIP levels between the two groups both in the early and the late measurements. Conclusion: Antenatal glucocorticoids (GCs) stimulate gastrin secretion in the fetus but not in the neonate. Contrary to this, corticosteroid effect on motilin is seen only postnatally following the introduction of enteral feeding. Glucocorticosteroids appear to have no effect on VIP levels. Plasma gastrin and motilin levels increase significantly following the introduction of enteral feeding regardless of the use of steroids.